One of the basic questions underlying the pathogenesis of cystic fibrosis (CF) is why these patients invariably develop infections with Pseudomonas aeruginosa. It is unclear how the "basic defect" in CF and the resultant abnormalities in electrolyte transport are related to the development of pulmonary infection. We plan to study the molecular interactions between CF epithelial cells in primary culture and genetically well characterized strains of Pseudomonas. We postulate that the CF epithelium presents either an altered cell surface receptor for Pseudomonas or increased numbers of receptors than are present in normal cells. Using monoclonal antibodies which block Pseudomonas adherence, we can map the binding epitopes on the Pseudomonas ligand, pilin. We can then use this and other monoclonal antibodies to identify the receptor on the epithelial cell which binds Pseudomonas. The receptors on CF cells and normals can then be directly compared. This should allow us to identify the specific component of CF epithelial cells which is responsible for Pseudomonas binding. We can then determine if the receptor is linked directly or indirectly with anion transport.